ライフサイエンスコーパス: beta-glucocerebrosidase

1 tein LIMP-2 is a specific binding partner of beta-glucocerebrosidase.

2 osphate-independent trafficking receptor for beta-glucocerebrosidase.

3 ensitive essential, lipid-processing enzyme, beta-glucocerebrosidase.

4 lamellar membranes and decreased activity of beta-glucocerebrosidase.

5 ivation of a pH-dependent hydrolytic enzyme, beta-glucocerebrosidase.

6 Finally, the activity of epidermal beta-glucocerebrosidase, a key lipid-processing enzyme,

7 beta-glucocerebrosidase activity and protein levels were

8 y available methodologies for measuring acid beta-glucocerebrosidase activity are primarily conducted

9 Concurrently, there was diminished beta-glucocerebrosidase activity at the stratum granulos

10 Twenty minutes postdose, beta-glucocerebrosidase activity increased over endogeno

11 Acid beta-glucocerebrosidase activity is measured in molecule

12 barrier recovery, attributable to decreased beta-glucocerebrosidase activity, assessed zymographical

13 By contrast, beta-glucocerebrosidase activity, which is responsible f

14 ellar membranes attributable to an increased beta-glucocerebrosidase activity.

15 c pH-dependent, ceramide-generating enzymes, beta-glucocerebrosidase and acidic sphingomyelinase, lea

16 assayed as inhibitor of the human lysosomal beta-glucocerebrosidase and as pharmacological chaperone

17 Activities of beta-glucocerebrosidase and steroid sulfatase, enzymes p

18 the activity of the lipid synthetic enzymes beta-glucocerebrosidase and steroid sulfatase, markers o

19 nzymes critical to stratum corneum function, beta-glucocerebrosidase and steroid sulfatase.

20 independent lysosomal targeting, binding to beta-glucocerebrosidase (beta-GCase) and directing it to

21 rmalities were attributable to a decrease in beta-glucocerebrosidase (beta-GlcCer'ase) and acidic sph

22 pression of the key lipid processing enzyme, beta-glucocerebrosidase (beta-GlcCer'ase), develops simi

23 ression also led to lysosomal transport of a beta-glucocerebrosidase endoplasmic reticulum retention

24 tion, motor exam score, sex, depression, and beta-glucocerebrosidase (GBA) mutation status were inclu

25 ylceramide catalyzed by the lysosomal enzyme beta-glucocerebrosidase (GBA).

26 n genetic disease caused by mutations in the beta-glucocerebrosidase (GBA1) gene that have been also

27 Mutations in the acid beta-glucocerebrosidase (GBA1) gene, responsible for the

28 Mutations within the lysosomal enzyme beta-glucocerebrosidase (GC) result in Gaucher disease a

29 P-2) plays a pivotal role in the delivery of beta-glucocerebrosidase (GC) to lysosomes.

30 ease (GD) results from mutations in the acid beta-glucocerebrosidase (GCase) encoding gene, GBA, whic

31 ions in the GBA1 gene that encodes lysosomal beta-glucocerebrosidase (GCase) represent an important r

32 Stabilization of misfolded mutant beta-glucocerebrosidase (GCase) represents an important

33 hypothesized that specific mutations in the beta-glucocerebrosidase gene (GBA) causing neuropathic G

34 ive disorder caused by mutations in the acid beta-glucocerebrosidase gene.

35 Lysosomal acid beta-glucocerebrosidase hydrolyzes glucocerebroside to g

36 Following infusion of recombinant human acid beta-glucocerebrosidase in mice, nonparenchymal cells ar

37 Activity of beta-glucocerebrosidase increased after PPARalpha-activa

38 ential binding among the different series of beta-glucocerebrosidase inhibitors.

39 lacental-derived or recombinant form of acid beta-glucocerebrosidase is targeted to the macrophages.

40 P-2-deficient fibroblasts led to a rescue of beta-glucocerebrosidase levels and distribution.

41 eled human placental-derived and recombinant beta-glucocerebrosidase (pGCR and rGCR, respectively).

42 ity to evaluate the efficacy of in vivo acid beta-glucocerebrosidase replacement therapy in animal mo

43 beta-glucocerebrosidase, the enzyme defective in Gaucher

44 They show that beta-glucocerebrosidase-the lysosomal enzyme defective i

45 Missorting of beta-glucocerebrosidase was also evident in vivo, as pro

46 om these mice indicated that the majority of beta-glucocerebrosidase was secreted.

47 sential for normal stratum corneum function, beta-glucocerebrosidase, which converts glucosylceramide

48 e found to be good inhibitors of recombinant beta-glucocerebrosidase with Ki values between 8.3 and 1